Implantable medical device for treating cardiac mechanical dysfunction by electrical stimulation

Abstract

The above-described methods and apparatus are believed to be of particular benefit for patients suffering heart failure including cardiac dysfunction, chronic HF, and the like and all variants as described herein and including those known to those of skill in the art to which the invention is directed. It will understood that the present invention offers the possibility of monitoring and therapy of a wide variety of acute and chronic cardiac dysfunctions. The current invention provides systems and methods for delivering therapy for cardiac hemodynamic dysfunction.

Description

[0001] This patent disclosure claims the benefit of provisional U.S. Patent Application Serial No. 60 / 315,316 filed Aug. 28, 2001 the entire contents of which are hereby incorporated by reference herein.[0002] This patent disclosure hereby incorporates by reference commonly assigned U.S. Pat. No. 6,438,408 which issued Aug. 20, 2002 and entitled, "IMPLANTABLE MEDICAL DEVICE FOR MONITORING CONGESTIVE HEART FAILURE," by Lawence J. Mulligan et al. and International Application No. PCT / US01 / 50276 invented by Deno et al. and entitled, "IMPLANTABLE MEDICAL DEVICE FOR TREATING CARDIAC MECHANICAL DYSFUNCTION BY ELECTRICAL STIMULATION."[0003] The present invention relates generally to implantable medical devices and more specifically to monitoring signs of acute or chronic cardiac mechanical dysfunction such as heart failure (HF), cardiogenic shock, pulseless electrical activity (PEA), or electromechanical dissociation (EMD), and providing appropriate therapies.[0004] Patients suffering from...

AI Technical Summary

Benefits of technology

[0027] Delivering pacing during the refractory period is a type of non-excitatory stimulation (NES) that causes the release of catecholamines such as norepinephrine within the tissue of the heart. This chemical release results in an increased contractility of the cardiac tissue, which in turn, results in increased cardiac output, fewer symptoms of heart failure and improved exertional capacity.

[0098] A second change is to increase the time between the later shocks in the sequence. With greater spacing, higher detection specificity would be possible and minimize the potential risk of shock-induced myocardial damage.

Problems solved by technology

As the disease progresses, the lack of cardiac output may contribute to the failure of other body organs, leading to cardiogenic shock, arrhythmias, electromechanical dissociation, and death.

Although these agents may be beneficial in specific settings, they require administration of a drug, often by intravenous route, with systemic side effects and the time-consuming involvement of skilled clinicians.

However, the SR continues to take up further calcium with the result that the subsequent cardiac cycle causes a large release of calcium from the SR and the myocyte contracts more vigorously.

However, determining the appropriate pacing parameters is difficult.

As a direct result of a tachycardia or as a sequela, cardiac function may deteriorate to the point of greatly reduced cardiac output and elevated diastolic pressure.

However, prior art systems have not achieved a comprehensive therapy regimen that coordinates these mechanisms in a manner that is both safe and effective.

One problem involves the dangers associated with delivering stimulation during a nonrefractory period to achieve PESP.

A second problem may be a shift in the magnitude of resulting potentiation or refractory interval due to the course of disease or medication.

These may lead to unacceptable levels of potentiation performance, or loss of effect altogether.

Another problem associated with PESP is that the added ventricular depolarization may cause the loss of AV conduction during the next cardiac cycle.

This results in loss of the next intrinsic depolarization in the ventricle.

The resulting pattern may be unstable, characterized by intermittent shifts between 2:1 and 1:1 conduction which may offset the other benefits provided by the PESP since ventricular filling is compromised.

This results in an extra systole that increases contractile function and stroke volume on subsequent contractions.

Institution of PESP therapy may result in intermittent 2:1 AV block.

Unfortunately, 2:1 conduction may produce a ventricular rate that is too slow where as 1:1 conduction with PESP may result in a ventricular rate that is too fast.

When PESP therapy is initiated, a 2:1 AV block typically occurs (and can be depicted with a second waveform "B") although the 2:1 AV block is often unstable.

The use, however, of a mechanical sensor such as a pressure sensor or an accelerometer to determine whether or not to apply therapy has the drawback in that external treatments of PEA / EMD such as cardiac chest compressions may introduce error into the physiologic signals, inhibiting or delaying therapy when it may be needed.

The vulnerable period represents a time period during which an electrical pulse delivered at, or above, a pre-determined amplitude has the risk of causing a VT or VF episode.

Further delays of the stimulation diminish the amount of potentiation.

Stimulation too early (i.e., prematurely) results in no additional potentiation at all since the myocardium is refractory.

However, the inventors have discovered that such a risk is quite low if single PESP pulses are delivered according to the safety lockout rule (briefly described above) and ACP coordination (also briefly described above).

Conduction to the ventricles is so rapid as to impair filling and ejection and as a result pressures and flows are typically impaired.

In the course of our research we increased the controller's gains which led to oscillation.

The devices analyze the effective heart rate and rhythm accordingly and do not falsely detect or treat tachyarrhythmias.

This is particularly the case with HF patients or other patients in whom the stiffness of the heart is increased, cardiac filling during the passive filling phase (T.sub.4-T.sub.7) and during atrial systole (T.sub.0-T.sub.1) is significantly limited.

These conduction defects give rise to great asynchrony between RV activation and LV activation.

Of course, such sensors must be rendered biocompatible and reliable for long-term use.

This therapy regimen causes a forced deceleration of the cardiac rhythm.

The heart tissue is not guaranteed sufficient time in diastole for good filling, coronary flow, and ion flux stabilization.

As a result, the peripheral pulse rate is variable, mechanical enhancement is less consistent, and the heart more prone to arrhythmias and metabolic intolerance.

This pattern is often unstable (see FIG. 8 above) and may result in effective ventricular rates that are too slow (brady) or too fast (tachy).

This approach helps when the result of the case depicted in FIG. 9B was an effective ventricular rate that was too slow or too irregular, but does not allow the subject's physiology to set heart rate, paces the atrium frequently, and may result in an excessive heart rate.

However, if ACP is delivered above threshold in this setting, this could raise the ventricular rate by conducting to the ventricles.

Furthermore, at these high heart rates PESP potentiation diminishes.

Heart rates this high are poorly tolerated and will further contribute to cardiac dysfunction, heart failure decompensation, and predispose a person subjected to such an effective heart rate to VT or VF.

Upon restoration of a more normal rhythm, the device may or may not re-enable automatic therapy delivery.

Therapies may also be disabled upon reaching a fixed number of therapy applications and require an external override to restart.

Without adequate blood flow, the heart will remain ischemic and the subject will likely die of PEA.

Conduction to the ventricles is so rapid as to impair filling and ejection and as a result pressures and flows are typically impaired (trace B).

This may be thought of as closing the loop but results in a slow response time.

In this patent disclosure, the inventors report that they increased the controller gain to the point where oscillations developed, an instability phenomenon well known in the area of feedback control.

The devices analyze the effective heart rate and rhythm accordingly and do not falsely detect or treat tachyarrhythmias.

As a result, a victim of sudden cardiac arrest oftentimes rapidly or eventually succumbs to cardiac dysfunction or EMD / PEA.

Images